A Hemodynamic Bridge from Echocardiography to Directly Measured Left Ventricular End-Diastolic Pressure: The Intermediate Role of Pulmonary Artery Diastolic Pressure in a Routine Catheterization Cohort.

Background

Noninvasive echocardiographic markers are widely used to estimate left ventricular filling pressure, but their relationship with directly measured left ventricular end-diastolic pressure (LVEDP) is often modest and context-dependent. Whether routinely available noninvasive findings reflect elevated LVEDP through an intermediate invasive pulmonary hemodynamic phenotype remains insufficiently characterized.

Objective

To evaluate the relationship of noninvasive echocardiographic and laboratory markers with directly measured LVEDP and to determine whether invasive pulmonary artery diastolic pressure (dPAP) functions as a hemodynamic bridge linking upstream noninvasive findings to elevated left ventricular filling pressure in a routine catheterization cohort.

Methods

This retrospective single-center observational study included patients undergoing routine cardiac catheterization with available direct LVEDP measurement and invasive pulmonary artery pressure data. Elevated LVEDP was defined as LVEDP ≥ 15 mmHg, and elevated dPAP as dPAP ≥ 24 mmHg. Noninvasive, bridge, and invasive validation models were evaluated using logistic regression, receiver operating characteristic analysis, calibration assessment, and bootstrap internal validation.

Results

A total of 75 patients had direct LVEDP data, 94 had invasive dPAP data, 83 had echocardiographic systolic pulmonary artery pressure (echo-sPAP), and 37 had pulmonary capillary wedge pressure (PCWP) measurements. Patients with elevated LVEDP had significantly higher creatinine (p = 0.026), dPAP (p = 0.043), and PCWP (p = 0.004). Echo-sPAP showed good discrimination for elevated dPAP, with an AUC of 0.791 (95% CI 0.695-0.888), supporting its role as an upstream noninvasive marker of invasive pulmonary hemodynamic burden. A noninvasive model combining echo-sPAP and creatinine showed modest discrimination for elevated LVEDP (AUC 0.664, 95% CI 0.522-0.806; Brier score 0.198), whereas an invasive validation model combining dPAP and creatinine showed better performance (AUC 0.734, 95% CI 0.617-0.850; Brier score 0.176). In bootstrap validation, the optimism-corrected AUCs were approximately 0.624 and 0.711, respectively. Although the invasive model performed numerically better, DeLong comparison did not show a statistically significant difference between the two models (p = 0.459).

Conclusions

Routinely available noninvasive echocardiographic and laboratory findings appear to relate to directly measured left ventricular filling pressure through an intermediate invasive pulmonary hemodynamic pattern. Echo-sPAP showed its strongest signal at the level of elevated dPAP, whereas dPAP combined with creatinine provided the most informative model for elevated directly measured LVEDP. These findings support a hypothesis-generating hemodynamic framework linking noninvasive assessment to directly measured filling pressure and may help inform noninvasive hemodynamic triage and physiological risk enrichment in selected clinical settings.